What you carry at this position in your DNA and what research says about it.
Metformin Response: 6/10 evidence, 10 publications.
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Sample genotype (not yours): G/G
Typical Metformin Clearance and Response
Standard clearance rates of metformin support a typical glucose-lowering response. Standard therapeutic doses are generally expected to perform as predicted by standard clinical guidelines.
What this genotype means: Typical metformin excretion rate; Standard blood sugar response; No altered cisplatin toxicity risk.
Sample genotype (not yours): A/A
Enhanced Metformin Response and Slower Clearance
Two copies of the A allele significantly delay metformin excretion, leading to a stronger glucose-lowering effect. Slower clearance may also increase the risk of rare medication-related side effects.
What this genotype means: Slower metformin excretion; Greater reduction in HbA1c levels; Favorable response to sulfonylurea combination.
Sample genotype (not yours): G/A
Slightly Enhanced Metformin Response
A single copy of the A allele may slightly delay metformin excretion, potentially enhancing its blood sugar-lowering effects. Response patterns can vary depending on individual metabolic factors.
What this genotype means: Slightly slower metformin clearance; Potential for enhanced glucose-lowering; No altered cisplatin toxicity risk.
Gene function and biological role
Gene Function: The SLC47A1 gene encodes the multidrug and toxin extrusion 1 (MATE1) protein, which acts as a critical cellular exporter. This transporter is primarily located in the membranes of liver and kidney cells, where it pumps various organic cations out of cells and into the bile or urine for excretion. Among its most notable substrates is metformin, the widely prescribed first-line medication for type 2 diabetes. By facilitating the elimination of metformin, MATE1 plays a central role in regulating the drug's active concentrations in the body. Variations in this gene can alter transporter activity, directly influencing how efficiently medications are cleared and how strongly they lower blood sugar levels.
Variant Impact: Located within the SLC47A1 gene, the rs2289669 intronic change has been widely studied for its impact on drug transport. This genetic variation is thought to influence the expression or function of the MATE1 transporter, thereby altering the rate at which metformin is excreted from the body. Carrying the minor A allele is associated with a reduced rate of metformin clearance, which can lead to higher drug levels and a more pronounced glucose-lowering effect. Researchers have also investigated this variant's role in the clearance of other therapeutic agents, such as cisplatin, though findings show no significant impact on cisplatin-induced kidney toxicity.
Key Insight: The minor A allele of this variant slows down the excretion of metformin, which can actually enhance the drug's ability to lower blood sugar levels.
Location: SLC47A1. Chromosome 17 · 17p11.2 · 19.6 Mb
Estimated prevalence by population
Global 47.5%; European 34.8%; African 83.8%; East Asian 25.9%; South Asian 25.4%; Americas 30.9%; Ashkenazi 23.5%; Finnish 41.3%; Middle Eastern 24.0%; Amish 45.3%.
Estimated GG genotype frequency.
Global 39.4%; European 48.4%; African 15.5%; East Asian 50.0%; South Asian 50.0%; Americas 49.4%; Ashkenazi 50.0%; Finnish 45.9%; Middle Eastern 50.0%; Amish 44.0%.
Estimated GA genotype frequency.
Global 13.1%; European 16.8%; African 0.7%; East Asian 24.1%; South Asian 24.6%; Americas 19.7%; Ashkenazi 26.6%; Finnish 12.8%; Middle Eastern 26.0%; Amish 10.7%.
Estimated AA genotype frequency.
Showing effects for G/G genotype
Pharmacogenomics
Diabetes Medication Response
Metformin Response. Evidence: 6/10. Source: PMID 22882994. Typical Response.
Sulfonylurea Response. Evidence: 6/10. Source: PMID 39005567. Typical Response.
Chemotherapy Response
Cisplatin Toxicity. Evidence: 3/10. Source: PMID 22569819. No Association.
Showing effects for A/A genotype
Metformin Response. Evidence: 6/10. Source: PMID 22882994. Enhanced Response.
Sulfonylurea Response. Evidence: 6/10. Source: PMID 39005567. Enhanced Response.
Showing effects for G/A genotype
Metformin Response. Evidence: 6/10. Source: PMID 22882994. Slightly Enhanced.
What this genotype means for the people who carry it
Sample genotype: GG (Homozygous)
Standard functioning of the MATE1 transporter is typical for those with two copies of the common G allele. Under these conditions, metformin is excreted from the body at a typical rate through the kidneys and liver. This standard clearance means that blood sugar-lowering effects generally align with typical clinical expectations. Some studies suggest that individuals with this genotype do not experience the enhanced glucose-lowering effects seen in carriers of the A allele. Clinical dosing strategies for type 2 diabetes medications typically apply here without genetic adjustments. Additionally, research indicates no altered risk for adverse events when undergoing platinum-based chemotherapy treatments like cisplatin. Overall, this genetic profile represents the baseline reference for metformin pharmacokinetics in the general population.
Typical metformin excretion rate; Standard blood sugar response; No altered cisplatin toxicity risk.
Sample genotype: AA (Homozygous)
Possessing two copies of the minor A allele is associated with a more pronounced reduction in MATE1 transporter function. Delayed excretion of metformin occurs as a result of this functional change, allowing the drug to persist in the body at higher active concentrations. Clinical trials have demonstrated that this slower clearance often translates to a significantly greater reduction in HbA1c levels. While this enhanced efficacy is highly beneficial for blood sugar control, the prolonged exposure can occasionally increase the risk of gastrointestinal side effects. Extremely slow clearance has been studied in connection with metformin-associated lactic acidosis in rare cases, though this remains an uncommon complication. Improved therapeutic response is also observed when metformin is combined with sulfonylureas. No altered risk of kidney toxicity has been observed during cisplatin chemotherapy treatments.
Slower metformin excretion; Greater reduction in HbA1c levels; Favorable response to sulfonylurea combination.
Sample genotype: GA (Heterozygous)
A mild reduction in MATE1 transporter activity is often observed with a single copy of the minor A allele. This subtle change can slightly slow down the rate at which metformin is cleared from the body. Consequently, the active drug remains in circulation slightly longer, which may enhance its therapeutic efficacy in lowering blood glucose. Clinical studies show mixed results, with some reporting a better response and others finding no significant difference compared to the typical genotype. Other genetic or lifestyle factors also play a role in overall drug response, explaining some of this variability. Favorable response patterns have also been noted in combination therapies involving sulfonylureas. No significant association has been found between this genotype and the risk of kidney damage during cisplatin chemotherapy.
Slightly slower metformin clearance; Potential for enhanced glucose-lowering; No altered cisplatin toxicity risk.
Variants with shared genetic architecture
rs8192675 · SLC2A2 Gene · Chr 3 · Diabetes Risk
rs622342 · SLC22A1 Gene · Chr 6 · Metformin Response
rs391300 · SRR Gene · Chr 17 · Diabetes Risk
Content updated August 2026.
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